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(1/15) Bellringer: Homeostasis 1. Define homeostasis. 2. Propose a role for each of the following in maintaining homeostasis: a. Receptor b. Integrator c. Effector Copyright © 2010 Pearson Education, Inc. (1/15) Partner BR: Fight-or-flight 1. What is the ligand? 2. What type of receptor does it bind? 3. What is the second messenger? 4. How does protein kinase A distribute the signal? 5. Which enzyme breaks down glycogen? 6. What is the cellular response? 7. How is this pathway an example of amplification? Copyright © 2010 Pearson Education, Inc. 29.1: Multicellular animals require a stable internal environment • Homeostasis: all body systems working together to maintain a stable internal environment • Regulatory systems consist of: 1. Receptor – receives stimulus & transmits sensory info to spinal cord & brain (central nervous system) – chemoreceptors, photoreceptors, thermoreceptors, & touch/pressure receptors 2. Integrator – processes sensory info & determines response – Brain sends out motor commands 3. Effector – carries out response – Muscles, organs, & glands Copyright © 2010 Pearson Education, Inc. Feedback Loop Copyright © 2010 Pearson Education, Inc. 29.2: Physiological regulation achieves homeostasis of the internal environment • Negative feedback: variation triggers response that corrects situation – response of effector negates stimulus, restoring homeostasis – The nervous & endocrine (hormones) systems operate thru negative feedback • Positive Feedback: response of the effector reinforces the change caused by the stimulus, moving the body away from homeostasis temporarily until the desired response is carried out – Ex: blood clotting process, childbirth Copyright © 2010 Pearson Education, Inc. Negative Feedback Copyright © 2010 Pearson Education, Inc. Positive Feedback: thrombin activation starts a positive feedback loop that leads to more thrombin formation from prothrombin; the ultimate response is fibrin formation to clot the break in the blood vessel Copyright © 2010 Pearson Education, Inc. Negative Feedback: Hormonal control (CH 30) • Blood calcium levels are regulated by 2 hormones: calcitonin & parathyroid hormone • Calcitonin is released by the thyroid when calcium levels are high, moving calcium into bones & increasing calcium loss at the kidney • Parathyroid hormone is released when levels are low, adding calcium to the blood Copyright © 2010 Pearson Education, Inc. Negative Feedback: Hormonal control • Blood glucose levels are regulated by 2 pancreas hormones: insulin & glucagon • Insulin is released when glucose levels are high, moving glucose out of the blood and into cells • Glucagon is released when levels are low, adding glucose to the blood from glycogen stores in the liver and muscle Copyright © 2010 Pearson Education, Inc. Cell Communication Poster Project Topics Research topics Toxin (1) Poison dart frog, Marine Cone Snails Plant (2) Phototropism (auxin), Ripening (ethylene) Immune (1) Drug (1) B-lymphocytes, T- lymphocytes Heroin, Ecstasy Human (1) Vision Bacteria (1) Disease (1) Clostridium botulinum neurotoxin (botulism) Diabetes/Insulin (healthy and faulty), Parkinson’s and calcium channels (healthy and faulty) Copyright © 2010 Pearson Education, Inc. (1/19) BR 1. What is a neurotransmitter? 2. Why are reflex reactions so FAST? Copyright © 2010 Pearson Education, Inc. CH 34: Neurons & Nervous Systems • Neurons respond rapidly to stimuli to maintain homeostasis A. Types & functions 1. Sensory neurons: receive stimuli & transmit info to CNS 2. Interneurons in brain & spinal cord process sensory info 3. Motor neurons: deliver commands from CNS to effector cells B. Structure • Dendrites – antenna-like extensions that receive stimuli from the environment or another neuron • Cell body (soma) – contains nucleus & organelles • Axon – carries outgoing signals called action potentials • Synaptic terminals – ends of axons where neurons communicate with effector cells Copyright © 2010 Pearson Education, Inc. 1. Label the cell body, axon, dendrites, synaptic terminals, and effector on your neuron diagram. 2. Draw a line that shows the direction in which information travels along a neuron. Copyright © 2010 Pearson Education, Inc. Structural Neurons 1. Multipolar neuron: • Most common neuron in brain & spinal cord • All motor neurons that synapse at skeletal muscles 2. Unipolar neurons: • Sensory neurons of peripheral nerves 3. Bipolar neurons: • Special sense organs (sight, smell, hearing) Copyright © 2010 Pearson Education, Inc. Reflexes • Reflex: automatic response to stimulus that bypasses the brain – Reflex arc: response opposes original stimulus 1. Stimulus activates sensory neuron 2. Integration by interneuron in spinal cord 3. Motor neuron carries command 4. Effector response Copyright © 2010 Pearson Education, Inc. Figure 8-28 Copyright © 2010 Pearson Education, Inc. A Flexor Reflex Figure 8-30 Copyright © 2010 Pearson Education, Inc. Stretch Reflex Figure 8-29 Copyright © 2010 Pearson Education, Inc. Membrane Potential • Membrane Potential – charge difference on either side of the plasma membrane – Resting Potential of neuron is negative (-70mV) because of Na+ / K+ pump • Uses ATP to actively transport 3 Na+ out and 2 K+ in Copyright © 2010 Pearson Education, Inc. Figure 34.5 Ion Transporters and Channels (Part 1) Na+–K+ pump (ATPase) Outside of cell Sodium– potassium pump 3 Na+ 2 K+ ATP ATP Pi K+ Inside of cell Copyright © 2010 Pearson Education, Inc. ADP Na+ K+ Pi Figure 34.5 Ion Transporters and Channels (Part 2) Na+–K+ channels Outside of cell Leak K+ channel Voltage-gated K+ channel Closed Closed Open Inside of cell Copyright © 2010 Pearson Education, Inc. Voltage-gated Na+ channel Open 3. Analyze the graph to define depolarization and repolarization. Copyright © 2010 Pearson Education, Inc. Action Potential • Action Potential: an electrical impulse sent by a neuron down its axon – occurs when a stimulus causes a neuron to depolarize (become less negative) to threshold (-60mV) – All-or-none principle: if an action potential begins, it will occur at the same magnitude every time; there is no variation in the size/strength of an action potential – 4 steps: Copyright © 2010 Pearson Education, Inc. 1. Stimulus causes a depolarization to threshold Copyright © 2010 Pearson Education, Inc. 2. Voltage-gated channels open, & Na+ rushes into the cell, causing further depolarization Copyright © 2010 Pearson Education, Inc. 3. Na+ channels close & K+ voltage-gated channels open • K+ rushes out, repolarizing the cell Copyright © 2010 Pearson Education, Inc. 4. Resting membrane potential (-70mV) restored Copyright © 2010 Pearson Education, Inc. Figure 34.7 The Course of an Action Potential (Part 2) Resting potential Threshold Resting membrane potential restored Undershoot Outside of cell Voltage-gated K+ channel Voltage-gated Na+ channels K+ channel Activation gate Inactivation gate Inside of cell Copyright © 2010 Pearson Education, Inc. Voltage-gated Na+ channels open Voltage-gated Na+ channels close & K+ channels open Action potentials travel much faster down axons insulated by myelin (figure b). Draw and label myelin on your neuron. Figure 8-9 Copyright © 2010 Pearson Education, Inc. Copyright © 2010 Pearson Education, Inc. Myelin is shown in red below, insulating the axon. In reality, the lipid-rich myelin has a glistening white look. Copyright © 2010 Pearson Education, Inc. Myelin-producing Schwann cells Site and direction of myelin growth Nodes of Ranvier Nucleus of Schwann cell (specialized glial cell) Mitochondria Axon Copyright © 2010 Pearson Education, Inc. Myelin is formed by 2 types of glia (support cells of the nervous system) (1/20) BR: Rabies The rabies virus infects the CNS through a mechanism called retrograde flow. A bite from a rabid animal initially injects the virus into peripheral tissues at the surface of the skin. With this in mind, answer the following. 1.What type of neuron does the virus initially infect? Copyright © 2010 Pearson Education, Inc. Synapses • Synapse – site where a neuron communicates w/ another cell – Presynaptic neurons transmit action potentials to postsynaptic neurons or effector cells (e.g., muscle cells) by releasing neurotransmitters • Neurotransmitters must bind to a specific receptor on the postsynaptic cell to have an effect – Can have an excitatory or inhibitory effect on the postsynaptic cell depending on receptor (e.g., epinephrine during fight-or-flight response) – effect also depends on balance of excitation/inhibition by different neurotransmitters Copyright © 2010 Pearson Education, Inc. Synapses • At a cholinergic synapse the neurotransmitter is acetylcholine 1. Ca++ trigger the presynaptic neuron to release acetylcholine (Ach) into the synaptic cleft 2. ACh binds to ligand-gated Na+ channels on the postsynaptic membrane, causing depolarization as Na+ enters the cell 3. Acetylcholinesterase breaks down ACh in the synaptic cleft into acetate & choline which are recycled back into the presynaptic cell Copyright © 2010 Pearson Education, Inc. Figure 8-11 Copyright © 2010 Pearson Education, Inc. Figure 8-11 Copyright © 2010 Pearson Education, Inc. Figure 8-11 Copyright © 2010 Pearson Education, Inc. Figure 8-11 Copyright © 2010 Pearson Education, Inc. Neuromuscular Junction (synapse of a neuron with a muscle cell) Copyright © 2010 Pearson Education, Inc. Copyright © 2010 Pearson Education, Inc. Thick filament (made of myosin) Thin filaments (made of actin) Thick filament (made of myosin) Copyright © 2010 Pearson Education, Inc. At rest, the active sites on actin molecules are blocked by tropomyosin, which is held in place by troponin. An arriving action potential triggers the release of Ca2+ (a 2nd messenger!) from the smooth ER… Ca2+ exposes active sites on actin molecules by binding to troponin Copyright © 2010 Pearson Education, Inc. Myosin heads from thick filaments bind to actin active sites forming cross-bridges Myosin head Myosin head Copyright © 2010 Pearson Education, Inc. Myosin heads all pivot towards the center of the muscle fiber, pulling thin filaments inward & causing contraction Figure 7-5 Copyright © 2010 Pearson Education, Inc. ATP causes myosin heads to detach Figure 7-5 Copyright © 2010 Pearson Education, Inc. ATP is hydrolyzed, and myosin is reactivated to bind to actin Figure 7-5 Copyright © 2010 Pearson Education, Inc. Copyright © 2010 Pearson Education, Inc. Exit Tetrodotoxin is a neurotoxin in puffer fish that blocks voltage-gated sodium channels in a neuron’s plasma membrane from opening. What effect would this have on the neuron’s function? Action Potential animation Copyright © 2010 Pearson Education, Inc. (1/21) Bellringer: Action Potential review 1. Mark on the graph in your notes when Na+ are entering the cell and when K+ are leaving the cell. Then describe what is happening in each of the 4 steps of an action potential detailed in the graph. Copyright © 2010 Pearson Education, Inc. (1/21) Bellringer 2. Nonspecific defenses (i.e, innate immunity) protect the body by responding to all possible pathogens the same way (does not involve producing antibodies to combat specific pathogens). What are some of our nonspecific defenses that protect us from infection? Copyright © 2010 Pearson Education, Inc. TYPE OF CELL FUNCTION Basophils (I, A) Release histamine; may promote development of T cells Eosinophils (A) Kill antibody-coated parasites Neutrophils (I) Stimulate inflammation; engulf and digest microorganisms Mast cells (I) Release histamine when damaged Monocytes (I, A) Develop into macrophages and dendritic cells Macrophages (I, A) Engulf and digest microorganisms; activate T cells Dendritic cells (A) Present antigens to T cells B lymphocytes (A) Differentiate to form antibodyproducing cells and memory cells T lymphocytes (A) Kill virus-infected cells; regulate activities of other white blood cells Natural killer cells (I) Attack and lyse virus-infected or cancerous body cells Copyright © 2010 Pearson Education, Inc. • White Blood Cells (leukocytes) defend the body against pathogens & abnormal cells Phagocytes Lymphocytes LYMPHOPOIESIS: lymphocytes formation • T cells are Thymusdependent • B cells complete their development in the Bone marrow Copyright © 2010 Pearson Education, Inc. Lymphoid Anatomy • Organs integral to defense are the lymph nodes, thymus, and spleen Copyright © 2010 Pearson Education, Inc. 31.1 Animals use Innate and Adaptive Mechanisms to Defend Themselves against Pathogens • Innate immunity: nonspecific defenses do not distinguish 1 threat from another; they’re indiscriminate! 1. Physical Barriers – skin, mucus, lysozyme, stomach acid 2. Phagocytes engulf pathogens thru endocytosis (phagocytosis) • Ex: Macrophages (also monocytes, neutrophils, eosinophils) 3. Natural Killer (NK) cells (a type of lymphocyte) attack cancer & virus-infected cells by detecting surface proteins called antigens Copyright © 2010 Pearson Education, Inc. Phagocytosis • Do not distinguish 1 threat from another; indiscriminate! 1. Physical Barriers – skin, mucus, stomach acid 2. Phagocytes • Macrophages & other phagocytes (neutrophils, eosinophils, microglia) • Diapedesis – squeeze b/w endothelial cells Phagocyte • Chemotaxis 3. Immunological Surveillance • NK cells attack foreign, abnormal (e.g., cancer), & virus-infected cells by detecting surface proteins called antigens (AG) Yeast cell Copyright © 2010 Pearson Education, Inc. Nonspecific Defenses 4. Complement proteins – assist phagocytes, activate inflammation, cause lysis of pathogens 5. Interferons – cytokines released by virus-infected cells that trigger antiviral defenses in neighboring cells (are these autocrine, paracrine, juxtacrine, or endocrine signals?) Copyright © 2010 Pearson Education, Inc. (1/21) Bellringer 3. Infection or injury leads to INFLAMMATION. Explain some of the familiar signs of inflammation (e.g., at a wound on the surface of your skin). Copyright © 2010 Pearson Education, Inc. Nonspecific Defenses 6. Inflammation – Mast cells release histamine & prostaglandins – Capillary permeability increases, causing swelling – Blood vessels dilate, increasing blood flow to the area – temperature increases, increases enzyme reaction rate (speeding recovery) • May lead to fever Copyright © 2010 Pearson Education, Inc. The Inflammatory Response Copyright © 2010 Pearson Education, Inc. The Inflammatory Response Copyright © 2010 Pearson Education, Inc. Innate Immunity is nonspecific Copyright © 2010 Pearson Education, Inc. (1/22) BR 1. Name 3 types of leukocytes (white blood cells) that provide nonspecific defense (innate immunity) for the human body, then explain the function of each. Yeast cell Copyright © 2010 Pearson Education, Inc. Axon Motor neuron Presynaptic cell (motor neuron) Muscle fiber Axon terminal Below is a diagram of a synapse between a neuron and a muscle cell. 2.What is the ligand released from the neuron? 3.What happens when the ligand binds to a receptor on the postsynaptic cell? Acetylcholine molecules in vesicle Na+ Action potential Ca2+ Synaptic cleft Acetylcholine receptor Na+ Postsynaptic cell (muscle cell) Copyright © 2010 Pearson Education, Inc. Adaptive Immunity • Cellular immunity: T cells respond to antigens bound to membrane receptors called MHC proteins – Class I MHC display antigens on cancer or virus-infected cells (say, “Hey! I’m foreign! Kill me!”) – Class II MHC display antigens on antigen-presenting cells like phagocytes (after phagocytosis) & B cells (say, “Hey! There’s an intruder! Kill them all!”) Copyright © 2010 Pearson Education, Inc. Cell with surface antigen Free antigens Phagocytosis Antigenpresenting cell Antigen presentation on Class II MHC Helper T cell (TH) Copyright © 2010 Pearson Education, Inc. RECOGNITION PHASE Cytokine release activates other cells Macrophages are antigenpresenting cells When MHC proteins display antigens to activate helper T cells, is it an example of autocrine, paracrine, endocrine, or juxtacrine signaling? Copyright © 2010 Pearson Education, Inc. Cellular Immunity a. Helper T Cells (TH) – activated by antigen-presenting cells • Stimulate B cells and cytotoxic T cells to divide • Divide into: – more TH cells – Memory T cells (TM): kept on reserve (for decades) in case of 2nd exposure b. Cytotoxic T cells (TC) destroy cells with specific antigen c. Regulatory T cells (Treg) – suppress immune response & mediate tolerance to self antigens Copyright © 2010 Pearson Education, Inc. Antigenpresenting cell Bind RECOGNITION PHASE Helper T cell (TH) Cytokines activate B cells & cytotoxic T cells (TC) TC cell B cell Cell with surface antigen B cells differentiate into plasma cells TC cell Antibodies Cytokines HUMORAL IMMUNITY Copyright © 2010 Pearson Education, Inc. CELULAR IMMUNITY ACTIVATION PHASE EFFECTOR PHASE Humoral (antibody-mediated) Immunity • Humoral (antibody) immunity: B cells produce antibodies in response to antigens & pathogens in fluids – Activated by TH cytokine secretion to divide & differentiate into: a. Plasma cells – secrete antibodies (i.e., immunoglobulins), proteins w/ specific antigenbinding sites b. Memory B cells – become plasma cells upon 2nd exposure to antigen Copyright © 2010 Pearson Education, Inc. Adaptive Immunity Copyright © 2010 Pearson Education, Inc. Copyright © 2010 Pearson Education, Inc. Copyright © 2010 Pearson Education, Inc. Figure 31.7 Immunoglobulin (antibody) structure Antigenic Antigendeterminants binding site Variable region of heavy chain Constant region of heavy chain Light chain Heavy chain Disulfide bonds Copyright © 2010 Pearson Education, Inc. Antigen Variable region of light chain Constant region of light chain Humoral Immunity – Antibody(immunoglobulin) classes: 1. IgM – 1st antibodies to be released by B cells 2. IgG – 80% of antibodies – fight bacteria & viruses; can cross placenta 3. IgA – in mucus, tears, saliva, breast milk 4. IgE – stimulates inflammation by binding to mast cells 5. IgD – bind antigens to surface of B cells involved in B cell activation Copyright © 2010 Pearson Education, Inc. Figure 31.8 Heavy-Chain Genes Genes encoding variable region V1, V2…V~100 (variable) genes DNA 1 2 3 4…100 D1, D2…D~30 (diversity) genes 1 Genes encoding constant region J1, J2…J6 (joining) genes 2…30 1…6 µ δ γ3 γ1 γ2β γ2α ε Cδ J2 D3 V21 Copyright © 2010 Pearson Education, Inc. Constant region of protein Variable region of protein α Heavy-Chain Gene Recombination and RNA Splicing during B cell development DNA rearrangement Variable region Constant region V D J segments Embryonic DNA μ VDJ joining B cell DNA V Transcription and RNA splicing μ D J Transcription Primary RNA transcript μ Splicing mRNA Translation Each B cell’s genome codes for a unique immunoglobulin Copyright © 2010 Pearson Education, Inc. V C segments D J μ Light chain Heavy chain δ Cytokines • Cytokines – local (paracrine) chemical signals – Interleukins – most diverse & important cytokines • ↑ T cell sensitivity & antibody production, enhance nonspecific defenses (inflammation, chemotaxis, phagocytosis, complement, etc.) – Interferons – Tumor necrosis factors – kill tumor cells & slow tumor growth – Phagocytic regulators – causes monocytes to transform into macrophages – Colony-stimulating factors – stimulate blood cell production Copyright © 2010 Pearson Education, Inc. Exit In adaptive immunity, antibodies are produced by B cells in response to antigen exposure. Explain the graph below, then propose an explanation for it. Copyright © 2010 Pearson Education, Inc. (1/25) BR: Adaptive Immunity If your group did not turn in the Control of Blood Glucose POGIL on Friday, get them out and review the last few questions as a group! 1. What is an MHC receptor? 2. What is the role of an antigen-presenting cell? 3. Why are B & T cells referred to as being specific? 4. HIV depletes the body’s supply of helper T cells. Why does this lead to AIDS (acquired immune deficiency syndrome)? Copyright © 2010 Pearson Education, Inc. BR 5. What type of molecule is shown below? 6. On your note sheet, label the antigen, antigen-binding site, variable regions, and constant regions on the diagram. Copyright © 2010 Pearson Education, Inc. Immunoglobulin (antibody) structure Antigenbinding site Variable region of heavy chain Constant region of heavy chain Antigen Variable region of light chain Constant region of light chain Copyright © 2010 Pearson Education, Inc. 31.3 The Adaptive Immune Response is Specific • Adaptive Immunity has 4 key features: 1. Specificity 2. Diversity 3. Tolerance (distinguishing self from nonself) 4. Memory • Primary response – takes 1-2 weeks for peak antibody levels • Secondary response – much stronger, faster response after subsequent encounters with a pathogen Copyright © 2010 Pearson Education, Inc. Immunological Memory • Primary response – takes 1-2 weeks for peak AB levels • Secondary response – Memory cells immediately proliferate upon binding to the antigen, preventing illness Copyright © 2010 Pearson Education, Inc. Immune Disorders • Immunological disorders – Autoimmune Disorders: immune response targets normal body cells (autoantibodies are made) • Ex.: multiple sclerosis, rheumatoid arthritis, Type I diabetes mellitus, Lupus, celiac disease – Immunodeficiency: immune system does not develop normally or is impaired • AIDS (Acquired immunodeficiency syndrome) – result of HIV (Human Immunodeficiency Virus) killing TH Copyright © 2010 Pearson Education, Inc. Immune Disorders – Allergies – inappropriate or excessive inflammatory response to antigens • Mast cells release histamine in response to allergens – Anaphylaxis: mast cells throughout body affected – shock may result from drop in blood pressure Copyright © 2010 Pearson Education, Inc. (1/25) BR: Adaptive Immunity 7. What is a vaccine? How do vaccines work? Copyright © 2010 Pearson Education, Inc. 31.3 The Adaptive Immune Response is Specific • Adaptive Immunity (Specific defenses) A. Active immunity–results from the production of antibodies • Natural: in response to natural exposure to antigens • Induced: in response to vaccines, which are dead or weakened pathogens that stimulate an immune response B. Passive immunity –transfer of antibodies from mother to offspring across placenta or in breast milk Copyright © 2010 Pearson Education, Inc. Immunological Memory Copyright © 2010 Pearson Education, Inc. HIV slowly depletes the body of TH, and AIDS begins when levels drop below a certain point. Opportunistic diseases are usually the cause of death in AIDS patients. Copyright © 2010 Pearson Education, Inc. The course of an HIV infection Copyright © 2010 Pearson Education, Inc. Anti-HIV antibody production takes months to build, and levels remain high for years. When levels drop due to TH depletion, AIDS sets in. Copyright © 2010 Pearson Education, Inc. Exit 1. HIV infects TH (helper T cells) by binding to the CD4 receptor on the surface of the cells. A coreceptor called CCR5 works with CD4 receptors and is necessary for HIV to enter the TH. Some people have TH with a CCR5 receptor that is smaller and does not make it to the surface of the cells due to a genetic mutation. What effect do you think this mutation has on people? 2. HIV tests measure the amount of anti-HIV antibodies in the blood (the purple line). If you test negative for HIV, why should you get another test 6-12 months later to be sure? Copyright © 2010 Pearson Education, Inc. (1/26) BR: Review for Test 1. What is occurring at #1 in the diagram below? Name the 2 molecules. 2. What activates or opens the transport protein channel that allows the secondary messengers to enter the cell? What type of diffusion is this? Copyright © 2010 Pearson Education, Inc. (1/26) BR 3. Give support for the claim that the cells located in the tip of the plant shoot detect the light by comparing the results from treatment group I with the results from group II and group III. 4. In groups IV and V, the tips of the plants are removed and placed back onto the shoot on either a permeable (IV) or impermeable (V) barrier. Using the results from treatment groups IV and V, describe TWO additional characteristics of the phototropism response. Copyright © 2010 Pearson Education, Inc. (1/26) BR 5. Predict the most likely consequence for a nursing infant who is exposed to an intestinal bacterial pathogen (e.g., Salmonella) to which the mother was exposed three months earlier. Explain your reasoning. Copyright © 2010 Pearson Education, Inc. (1/26) BR 6. Draw a diagram similar to the one below for ONE of the NEGATIVE feedback mechanisms in #12-13 of your Feedback Mechanisms POGIL. Copyright © 2010 Pearson Education, Inc. (1/26) BR Relay molecules and secondary messengers have essentially the same jobs in signal transduction pathways. However, relay molecules are almost always proteins that require activation. They are large and do not diffuse through the cell quickly. Secondary messengers on the other hand are small, water soluble molecules that can diffuse quickly. They may or may not need activation before they are able to move the signal on to the next step in the process. Cyclic AMP (cAMP) and calcium ions (Ca2+) are common secondary messengers in human systems. 7. Within an organism it is critical that signals between cells are very specific. For example, if ligand A is meant to activate immune system cells to reproduce in response to an infection, it should not also cause other cells to grow as if they had received a growth hormone. When a ligand is released, what prevents all of the cells in the body from being affected? Copyright © 2010 Pearson Education, Inc. (1/26) BR: Refer to the handout for #8-9. 8. Which of the following is a valid interpretation of the experimental results that explains how individuals with type 2 diabetes differ from individuals without diabetes? a. The relatively low levels of glucose uptake in individuals with type 2 diabetes indicate that mobilization of GLUT4 to the cell surface is reduced in muscle cells of those individuals. b. The relatively low levels of glucose uptake in individuals with type 2 diabetes indicate that no functional GLUT4 protein is produced in the muscle cells of those individuals. c. The absence of activated insulin receptors in individuals with type 2 diabetes indicates that no insulin is secreted by the pancreatic cells of those individuals. d. The absence of activated IRS-1 in individuals with type 2 diabetes indicates that no functional insulin receptor protein is produced in the muscle cells of those individuals. Copyright © 2010 Pearson Education, Inc. (1/26) BR 9. Based on the experimental results, which of the following describes the most likely defect in muscle cells of patients with type 2 diabetes? a. Insulin receptor proteins do not reach the cell surface. b. Insulin does not activate its receptor. c. IRS-1 activation is reduced at high insulin concentrations. d. GLUT4 blocks glucose from entering cells. Copyright © 2010 Pearson Education, Inc.